Research Topic

Targeting α-synuclein in Parkinson’s Disease and Multiple System Atrophy

About this Research Topic

Parkinson’s disease (PD) and multiple system atrophy (MSA) are progressive diseases that manifest through motor (e.g. parkinsonism) and non-motor (e.g. autonomic failure) symptoms. PD and MSA belong to the devastating neurodegenerative disorders known as α-synucleinopathies as both exhibit abnormal deposits of α-synuclein in the cytoplasm. PD exhibits the inclusions primarily in neurons (Lewy bodies), whereas glial cytoplasmic inclusions are most common in MSA. To date, it is not clear why α-synuclein metabolism is dysregulated and represents the main component of these pathological aggregates. An unresolved issue is why α-synuclein positive inclusions predominantly occur in neurons in PD and in oligodendroglial cells in MSA. However, the leading role of α-synuclein contributing to α-synucleinopathy characteristics and disease progression is definite as it mediates disruption of cellular homeostasis and neuronal cell death when being dysregulated. Currently no effective treatment to stop the progression of the diseases is available. Different therapeutic approaches targeting α-synuclein are emerging, including e.g. immunotherapy and aggregation inhibitors, with promising results.

In this Research Topic we focus on therapeutic approaches that target the reduction of α-synuclein inclusions in neurons and glial cells, as well as neuronal death induced by α-synuclein toxicity. Furthermore, an in-depth understanding why and how α-synuclein aggregates in the different cell types in PD and MSA develop is very important and should be covered in the current Research Topic, as it is also the basis for the development of new therapeutic approaches. Furthermore, for the correct diagnosis of PD and MSA and especially for the discrimination of these two diseases we are interested in diagnostic methods using α-synuclein as predictive marker.

Topic Editors welcome clinical or translational Research Articles, Reviews, Mini-Reviews, Perspectives or Opinions that cover, but are not limited to, the following topics:
• α-synuclein toxicity in PD and/or MSA
• aggregation properties of α-synuclein in neurons and/or glial cells
• α-synuclein aggregation initiation in PD and/or MSA
• α-synuclein as diagnostic, predictive marker for PD and MSA, and for the discrimination of PD and MSA (e.g. biomarker studies in blood, cerebrospinal fluid; MRI studies etc)
• therapeutic approaches targeting α-synuclein toxicity or aggregation properties
• immunogenicity of α-synuclein aggregates


Keywords: α-synuclein, multiple system atrophy (MSA), Parkinson’s disease (PD), Lewy bodies (LBs), glial cytoplasmic inclusions (GCIs)


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Parkinson’s disease (PD) and multiple system atrophy (MSA) are progressive diseases that manifest through motor (e.g. parkinsonism) and non-motor (e.g. autonomic failure) symptoms. PD and MSA belong to the devastating neurodegenerative disorders known as α-synucleinopathies as both exhibit abnormal deposits of α-synuclein in the cytoplasm. PD exhibits the inclusions primarily in neurons (Lewy bodies), whereas glial cytoplasmic inclusions are most common in MSA. To date, it is not clear why α-synuclein metabolism is dysregulated and represents the main component of these pathological aggregates. An unresolved issue is why α-synuclein positive inclusions predominantly occur in neurons in PD and in oligodendroglial cells in MSA. However, the leading role of α-synuclein contributing to α-synucleinopathy characteristics and disease progression is definite as it mediates disruption of cellular homeostasis and neuronal cell death when being dysregulated. Currently no effective treatment to stop the progression of the diseases is available. Different therapeutic approaches targeting α-synuclein are emerging, including e.g. immunotherapy and aggregation inhibitors, with promising results.

In this Research Topic we focus on therapeutic approaches that target the reduction of α-synuclein inclusions in neurons and glial cells, as well as neuronal death induced by α-synuclein toxicity. Furthermore, an in-depth understanding why and how α-synuclein aggregates in the different cell types in PD and MSA develop is very important and should be covered in the current Research Topic, as it is also the basis for the development of new therapeutic approaches. Furthermore, for the correct diagnosis of PD and MSA and especially for the discrimination of these two diseases we are interested in diagnostic methods using α-synuclein as predictive marker.

Topic Editors welcome clinical or translational Research Articles, Reviews, Mini-Reviews, Perspectives or Opinions that cover, but are not limited to, the following topics:
• α-synuclein toxicity in PD and/or MSA
• aggregation properties of α-synuclein in neurons and/or glial cells
• α-synuclein aggregation initiation in PD and/or MSA
• α-synuclein as diagnostic, predictive marker for PD and MSA, and for the discrimination of PD and MSA (e.g. biomarker studies in blood, cerebrospinal fluid; MRI studies etc)
• therapeutic approaches targeting α-synuclein toxicity or aggregation properties
• immunogenicity of α-synuclein aggregates


Keywords: α-synuclein, multiple system atrophy (MSA), Parkinson’s disease (PD), Lewy bodies (LBs), glial cytoplasmic inclusions (GCIs)


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

12 July 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

12 July 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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